Indeed, there is increasing recognition of the potential of mitochondrial-derived nucleic acids (mtNA) to act as agonists of the IFN signaling machinery, possibly contributing to complex autoinflammatory diseases such as systemic lupus erythematosus (SLE) (17), as well as neurodegeneration (18, 19) and cancer (20, 21). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.